Ajmaline-Induced Slowing of Conduction in the Right Ventricular Outflow Tract Cannot Account for ST Elevation in Patients With Type I Brugada ECG
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- Brugada syndrome
- cardiac electrophysiology
- sudden cardiac death
- sudden infant death
See Article by Leong et al
The Brugada syndrome (BrS), and more recently the early repolarization syndrome (ERS), have been associated with the development of prominent J waves and a risk for development of polymorphic ventricular tachycardia and ventricular fibrillation, leading to sudden cardiac death.1,2 The electrocardiographic and arrhythmic manifestations of these syndromes generally manifest in young adults and occasionally in infants, leading to sudden infant death syndrome.3–5 The region of the heart most affected in BrS is the anterior right ventricular (RV) outflow tract (RVOT), accounting for why the accentuated J wave typically appear, as a coved-type ST-segment elevation, in the right precordial leads, V1-V3 (see Antzelevitch and Yan2 for references).
The electrocardiographic J wave is thought to be inscribed as a consequence of transmural differences in the manifestation of the action potential (AP) notch (Figure 1). This distinction is due to the presence of a prominent transient outward current (Ito) in the epicardium but not endocardium of the RVOT. This heterogeneity gives rise to a net inward current during the early phases of the AP that inscribe the J wave or ST-segment elevation.6 The available data suggest that an outward shift in the balance of currents active during phases 1 and 2 of the RV epicardial AP via either a reduction of inward current (INa or ICa) or increase in outward current (Ito, IKr, or IK-ATP) allows the intrinsically prominent Ito in RV epicardium to accentuate phase 1 repolarization. When phase 1 repolarizes to a voltage below that needed to activate the L-type Ca+2 channels, the Ca+2 channels fail to activate, resulting in loss of the AP plateau in the RV subepicardial cells where Ito is most prominent. …